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Biochemical markers of cerebrovascular injury in sleep apnoea syndrome

¹ Dept of Psychiatry and Psychotherapy, University Göttingen, Göttingen, ² Dept of Pulmology, Evangelic Hospital Göttingen-Weende, Bovenden and ³ Dept of Neurology of the University Ulm, Ulm, Germany

CORRESPONDENCE: W. Jordan, Psychiatrische Klinik, Universität Gôttingen, Von Sieboldstr. 5, 37075, Gôttingen, Germany. Fax: 49 551393887. E-mail: wjordan@gwg.de

Keywords: biochemical marker, ß-trace, neuron-specific enolase, sleep apnoea syndrome, stroke, S-100ß

Received: June 20, 2001
Accepted February 11, 2002

Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy.

Therefore, in 10 patients with mild SAS (age 50.8±9.9 yrs, respiratory disturbance index (RDI) 18±3.6, lowest arterial oxygen saturation (min S_a,O2) 80.5±4.06%) and nine patients with severe SAS (age 50.3±11.5 yrs, RDI 75.4±21.7, min S_a,O2 56.56±14.58%), serum concentrations of neuron-specific enolase (NSE), S-100ß protein, and ß-trace were measured just before and after sleep using commercially available assays.

Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS.

Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100ß, neuron-specific enolase and ß-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome.